A neurobehavioral analysis of the satiety effect of pancreatic glucagon is proposed. This research contributes to an understanding of the physiological control of food intake, which is a major problem in the psychobiology of motivated behavior and its solution is a prerequisite for the development of effective clinical control of obesity. Exogenous glucagon administration has been shown to suppress food intake in humans and experimental animals. The behavioral changes leading to this suppression and their neural and physiologic controls, however, remain unclear. Experiments will therefore be made with rats to determine whether glucagon suppresses food intake by eliciting the behavioral sequence typical of postprandial satiety and to determine whether glucagon has a specific satiety effect for food. These experiments will employ an objective and sensitive behavioral rating system developed in this laboratory. The potency of glucagon's satiety effect will be tested in sham feeding rats, in which gastrointestinal and postabsorptive food stimuli are eliminated. This preparation will also be used to test the relation between glucagon's effects on hepatic glycogenolysis and its satiety effect in order to identify the nature of the satiety signal generated by glucagon. The effect of total abdominal vagotomy and of specific hepatic vagotomy on glucagon's satiety effect will be tested to determine the site of the satiety signal. The effects of administration of nutrient glucagon secretogues will be tested to determine whether manipulation of endogenous glucagon can elicit satiety. Finally, the effect of glucagon administration in obesity will be tested in two animal models of obesity, the hypothalamic hyperphagic rat and the genetically obese ob/ob mouse. It is hoped this research will advance understanding of the control of feeding behavior, to stimulate further research and provide a possible rationale for development of a means for clinical management of obesity.